Figure 1.

Cardiomyocyte‐specific overexpression of CYP2J2 attenuated myocardial hypertrophy and remodeling in vivo. AMPKα2^+/+ mice were injected in the caudal vein with rAAV9‐CYP2J2. After 2 weeks, mice were exposed to continuous infusion of Ang II or a saline control for 14 days (8–10 mice for each group). (A) Left, gross morphology of adult hearts AMPKα2^+/+ mice 2 weeks after Ang II infusion. Scale bar: 1 mm. Right, heart weight: body weight ratios of adult WT mice after infusion with Ang II or saline control for 2 weeks. (B) Left, H&E staining of sections of adult hearts from AMPKα2^+/+ mice after infusion with Ang II or saline control for 2 weeks (Scale bar: 100 μm). Right, quantification of the size of cardiomyocytes by measurement of the cross‐sectional area on H&E‐stained sections. More than 200 cells from four different hearts were analyzed per group. (C) Left, masson trichrome staining of adult hearts from AMPKα2^+/+ mice after infusion with Ang II or saline control for 2 weeks. The blue area indicates collagen fibers. Scale bar: 1 mm. Right, quantification of the rate of cardiac fibrosis by measurement of the area of collagen deposition. (D) RT–PCR analyses of relative expression of ANP, BNP, β‐MHC, and ACTA1 genes from the hearts of mice exposed to the indicated conditions. (E) ELISA analysis showing the expression of ANP in plasma from AMPKα2^+/+ mice (n = 4–5 for each group). (F) Left, Western blot analyses showing the expression of the ANP protein in Ang II and Ang II+CYP2J2 groups. GAPDH was used as a loading control. Right, the intensity of the Western blot signal was quantified and is shown as relative protein expression after normalization to GAPDH. (G) Representative images of echocardiograms. (H) LVPW;s. (I) LV ejection fraction. (J) LV fractional shortening. The data represent the mean ± SEM from at least four independent experiments (*P < 0.05 vs. control group; ^$ P < 0.05 vs. control group; ^# P < 0.05 vs. Ang II group).